Limitation of angiography to identify the culprit plaque in acute myocardial infarction with coronary total occlusion utility of coronary plaque temperature measurement to identify the culprit plaque.

OBJECTIVES: The purpose of this study was to test the hypothesis that the maximal temperature (Tmax) site, as measured by thermal wire, coincides with the culprit plaque by intravascular ultrasound (IVUS) in patients with acute myocardial infarction (AMI). BACKGROUND: Subsequent thrombosis developing to the proximal region from the site of plaque rupture or erosion can potentially complicate the ability of coronary angiography to identify the accurate culprit plaque in patients with coronary total occlusion. METHODS: In 45 consecutive patients with a first anterior AMI, the Tmax site by thermal wire and the culprit plaque by IVUS were evaluated in the left anterior descending coronary artery (LAD). RESULTS: Twenty-five patients had LAD total occlusion, and the remaining 20 had LAD reperfusion. In both groups of patients, the Tmax site was significantly more distal to the angiographically most stenotic site or occlusive site (reperfusion: mean distance [MD] = 1.1 mm distal, 95% confidence interval [CI] 0.3 to 1.9 mm, p = 0.01; total occlusion: MD = 8.8 mm distal, 95% CI 8.0 to 9.6 mm, p < 0.0001). The culprit plaques by IVUS approximately coincided with those by angiography or thermal wire in patients with reperfusion. However, the angiographic occlusive site was significantly more proximal to the culprit plaque by IVUS (MD = 9.2 mm, 95% CI 7.9 to 10.6 mm, p < 0.0001), but the Tmax site coincided with the culprit plaque by IVUS (MD = 0.3 mm distal, 95% CI 0.3 mm proximal to 1.0 mm distal, p = 0.293) in patients with total occlusion. CONCLUSIONS: Temperature measurement of coronary plaque enables accurate localization of the culprit plaque in AMI with coronary total occlusion.     

Assessment of culprit lesion morphology in acute myocardial infarction: ability of optical coherence tomography compared with intravascular ultrasound and coronary angioscopy.

OBJECTIVES: The aim of the present study was to evaluate the ability of optical coherence tomography (OCT) for assessment of the culprit lesion morphology in acute myocardial infarction (AMI) in comparison with intravascular ultrasound (IVUS) and coronary angioscopy (CAS). BACKGROUND: Optical coherence tomography is a new intravascular imaging method with a high resolution of approximately 10 microm. This may allow us to assess the vulnerable plaques in detail in vivo. METHODS: We enrolled 30 patients with AMI, and analyzed the culprit lesion by OCT, CAS, and IVUS. RESULTS: The average duration from the onset of symptom to OCT imaging was 3.8 +/- 1.0 h. The incidence of plaque rupture observed by OCT was 73%, and it was significantly higher than that by CAS (47%, p = 0.035) and IVUS (40%, p = 0.009). Furthermore, OCT (23%) was superior to CAS (3%, p = 0.022) and IVUS (0%, p = 0.005) in the detection of fibrous cap erosion. The intracoronary thrombus was observed in all cases by OCT and CAS, but it was identified in 33% by IVUS (vs. OCT, p < 0.001). Only OCT could estimate the fibrous cap thickness, and it was 49 +/- 21 microm. The incidence of thin cap fibroatheroma (TCFA) was 83% in this population by OCT. CONCLUSIONS: Optical coherence tomography is a feasible imaging modality in patients with AMI and allows us to identify not only plaque rupture, but also fibrous cap erosion, intracoronary thrombus, and TCFA in vivo more frequently compared with conventional imaging techniques.     

Angiographic no-reflow phenomenon and plaque characteristics by virtual histology intravascular ultrasound in patients with acute myocardial infarction

OBJECTIVE: This study aimed to evaluate the relationship between the occurrence of the angiographic no-reflow phenomenon in patients with acute myocardial infarction (AMI) and the preintervention plaque composition as assessed by virtual histology intravascular ultrasound (VH-IVUS). BACKGROUND: The angiographic no-reflow phenomenon is an adverse prognostic factor in patients with AMI. METHOD: We enrolled consecutive 50 patients with ST-elevation AMI was treated by primary stent implantation. All culprit lesions were imaged by VH-IVUS before stent implantation. The angiographic no-reflow phenomenon was defined as a decrease in final TIMI flow grade compared with TIMI flow grade before stent implantation. RESULTS: Eight of 50 patients developed angiographic no-reflow after stent implantation. Gray-scale intravascular ultrasound (IVUS) showed significantly larger external elastic membrane volume and plaque burden in the no-reflow group. VH-IVUS showed a trend toward larger percentage of fibro-fatty plaque volume in the no-reflow group than in the reflow group (23.1 +/- 3.5 vs. 17.0 +/- 1.1%, P = 0.05). The presence of "marble"-like image, mainly consisting of fibro-fatty and fibrous plaque (plaque volume of fibro-fatty + fibrous >80% and containing fibro-fatty plaque volume >10%) was associated with angiographic no-reflow (P = 0.02). Corrected TIMI frame counts of the cases with "marble"-like image were significantly larger than the cases without it (46.8 +/- 5.6 vs. 27.4 +/- 2.3, P = 0.01). CONCLUSION: The culprit lesions with large plaque burden, or with "marble"-like image by VH-IVUS, are associated with the angiographic no-reflow phenomenon in patients with AMI.     

Relation of atherothrombosis burden and volume detected by intravascular ultrasound to angiographic no-reflow phenomenon during stent implantation in patients with acute myocardial infarction

This study investigated the mechanism of occurrence of the no-reflow phenomenon during stent implantation in patients with acute myocardial infarction (AMI) using intravascular ultrasound (IVUS) with volumetric analysis. Of 70 patients with AMI who underwent IVUS-guided stent implantation within 24 hours of symptom onset, 12 developed decreased Thrombolysis In Myocardial Infarction flow grade during stent implantation and without subsequent restoration to Thrombolysis In Myocardial Infarction flow grade before stenting. External elastic membrane cross-sectional area and maximum diameter at the culprit lesion as measured by IVUS before stent implantation were significantly larger in the no-reflow group (n = 12) than in the normal reflow group (n = 58; 20.1 +/- 6.5 vs 16.4 +/- 4.3 mm2, p = 0.015 for cross-sectional area and 5.2 +/- 0.9 vs 4.8 +/- 0.6 mm, p = 0.049 for maximum diameter). Plaque volume, volumetric plaque burden (plaque volume/external elastic membrane volume), and change in plaque volume during stent implantation (plaque volume after vs before) were significantly greater in the no-reflow group than in the normal reflow group (239 +/- 142 vs 178 +/- 72 mm3, p = 0.030; 0.76 +/- 0.07 vs 0.71 +/- 0.06, p = 0.010; and -46 +/- 63 vs -11 +/- 37 mm3, p = 0.013, respectively). In conclusion, high atherothrombotic burden and decreased plaque volume as detected by IVUS may be risk factors for development of the no-reflow phenomenon during stent implantation in patients with AMI.     

Circadian variation of plaque rupture in acute myocardial infarction

Studies have reported a circadian variation in the onset of acute myocardial infarction (AMI). Pathologic studies have revealed that plaque rupture is 1 of the major causes of AMI, but none of these has looked specifically at the circadian variation of plaque rupture. The aim of this study was to use intravascular ultrasound (IVUS) to investigate the circadian variation of plaque rupture in AMI. This study included 174 consecutive patients with AMI who underwent preinterventional IVUS. All patients were assigned to either a rupture group or a nonrupture group according to the preinterventional IVUS. In the 81 patients (47%) in the rupture group, the frequency of the onset of AMI increased significantly in the period from 6 A.M. to 12 P.M. compared with all other time periods (p <0.05). The clinical features of AMI in the rupture group were characterized as occurring significantly more at rest (67% vs 31%, p <0.01) and after significantly less preinfarction angina (22% vs 57%, p <0.01) compared with the nonrupture group. A different circadian variation was identified in the nonrupture group, characterized as a significant nocturnal nadir (12 to 6 A.M. compared with all other periods, p <0.05). The circadian variation of AMI is the result of a morning increase in incidence of plaque rupture.     

Association between hyperglycemia and the no-reflow phenomenon in patients with acute myocardial infarction

OBJECTIVES: We investigated the association between hyperglycemia and the no-reflow phenomenon in patients with acute myocardial infarction (AMI). BACKGROUND: Hyperglycemia is associated with increased risks of heart failure, cardiogenic shock, and death after AMI, but its underlying mechanism remains unknown. METHODS: A total of 146 consecutive patients with a first AMI were studied by intracoronary myocardial contrast echocardiography (MCE) after successful reperfusion within 24 h after symptom onset. Two-dimensional echocardiography was recorded on day 1 and three months later to determine the change in the wall motion score (DeltaWMS; sum of 16 segmental scores; dyskinesia = 4 to normokinesia = 0). RESULTS: The no-reflow phenomenon was found on MCE in 49 (33.6%) of 146 patients; their glucose level on hospital admission was significantly higher than that of patients who did not exhibit this phenomenon (209 +/- 79 vs. 159 +/- 56 mg/dl; p < 0.0001). There was no difference in glycosylated hemoglobin or in the incidence of diabetes mellitus between the two subsets. The no-reflow phenomenon was more often observed in the 75 patients with hyperglycemia (>/=160 mg/dl) than in those without hyperglycemia (52.0% vs. 14.1%; p < 0.0001). Patients with hyperglycemia had a higher peak creatine kinase level (2,497 +/- 1,603 vs. 1,804 +/- 1,300 IU/l; p = 0.005) and a lower DeltaWMS (3.7 +/- 4.8 vs. 5.7 +/- 4.3; p = 0.01) than did those without hyperglycemia. The blood glucose level was an independent prognostic factor for no reflow, along with age, gender, absence of pre-infarction angina, complete occlusion of the culprit lesion, and anterior AMI. CONCLUSIONS: Hyperglycemia might be associated with impaired microvascular function after AMI, resulting in a larger infarct size and worse functional recovery.     

Relation of stent overexpansion to the angiographic no-reflow phenomenon in intravascular ultrasound-guided stent implantation for acute myocardial infarction

The angiographic no-reflow phenomenon is observed in some patients during stent implantation for acute myocardial infarction (AMI). We attempted to clarify the influence of stent overexpansion and plaque morphology on the angiographic no-reflow phenomenon in AMI patients who underwent intravascular ultrasound (IVUS)-guided stent implantation. We assessed the thrombolysis in myocardial infarction (TIMI) flow grade in the coronary angiographic findings, and quantitative and qualitative IVUS findings, in a total of 90 patients who underwent IVUS-guided stenting for AMI. The patients were divided into two groups according to the stent-to-artery ratio: overexpansion group (ratio 1.2) and non-overexpansion group (ratio <1.2). Angiographic no-reflow (defined as TIMI flow grade <3) in stent implantation was observed in 15 patients (17%). Angiographic no-reflow was more frequently observed in the overexpansion group than in the non-overexpansion group (32% vs 11%, P = 0.0312). Patients with no-reflow had more lipid pool-like images or fissure/dissection than those without. In the overexpansion group, a lipid pool-like image and fissure/dissection were more frequently observed in patients with no-reflow. The rate of target lesion revascularization (TLR) in the overexpansion group was significantly lower than that in the non-overexpansion group during the follow-up period (10% vs 18%, P = 0.0476), but the incidence of pump failure in the overexpansion group was higher than that in the non-overexpansion group during the hospital course (28% vs 14%, P = 0.0358). Stent overexpansion in AMI patients is related to a higher incidence of angiographic no-reflow, especially if the lesion has a lipid pool-like image or fissure/dissection, although there is a tendency for lower TLR.     

Acquired ventricular septal defect during acute myocardial infarction: analysis of 38 unoperated necropsy patients and comparison with 50 unoperated necropsy patients without rupture

Thirty-eight patients (24 men and 14 women) with an acquired ventricular septal defect during acute myocardial infarction (AMI) (rupture group) were studied and their clinical and necropsy findings were compared with 50 patients who died during their first AMI without rupture (nonrupture group). The frequency of systemic hypertension (54 vs 52%), angina pectoris (28 vs 22%) and congestive heart failure (5 vs 0%) before the fatal AMI was similar for both rupture and nonrupture groups. Mean heart weights for men (498 vs 526 g) and women (397 vs 432 g) with and without septal rupture also were insignificantly different. Whereas previous studies of fatal AMI cases have shown that 50% of cases of fatal AMI without rupture have left ventricular scars, only 4 (10%) of the rupture cases had a left ventricular scar before the infarct that ruptured. The rupture group had a significantly more frequent (p less than 0.01) posterior location of the infarcts (74 vs 40%) and, therefore, a higher frequency of associated right ventricular infarcts 50 vs 18%). The number of 3 major (right, left anterior descending and left circumflex) epicardial coronary arteries narrowed at some point greater than 75% in cross-sectional area of atherosclerotic plaque was the same in both groups. The percent of these 3 arteries totally occluded or nearly so (greater than 95% in cross-sectional area) by plaque was significantly less (p less than 0.001) in the rupture group compared with the nonrupture group (9 of 99 arteries [9%] vs 38 of 144 arteries [26%]).(ABSTRACT TRUNCATED AT 400 WORDS)     

Multiple plaque rupture and C-reactive protein in acute myocardial infarction

OBJECTIVES: This study sought to investigate the relationship between multiple plaque ruptures, C-reactive protein (CRP), and clinical prognosis in acute myocardial infarction (AMI). BACKGROUND: Several studies have demonstrated that ruptured or vulnerable plaques exist not only at the culprit lesion but also in the whole coronary artery in some acute coronary syndrome (ACS) patients. Recent studies have reported that a ruptured plaque at the culprit lesion is associated with elevated CRP, which indicates a poor prognosis in patients with ACS. METHODS: We performed intravascular ultrasound in 45 infarct-related arteries and another 84 major coronary arteries in 45 first AMI patients. RESULTS: Plaque rupture was observed in 21 patients (47%) at the culprit site. Intravascular ultrasound revealed 17 additional plaque ruptures at remote sites in 11 patients (24%). Patients with multiple risk factors were more frequently found in our multiple-plaque rupture patients compared with single-plaque rupture or nonrupture patients (82% vs. 40% vs. 29%, p = 0.01). High-sensitive CRP levels had a positive correlation with the number of plaque ruptures (p < 0.01). All culprit lesions were successfully treated by percutaneous coronary intervention. Patients with multiple plaque rupture showed significantly poor prognosis compared with others (p = 0.01). CONCLUSIONS: Multiple plaque rupture is associated with systemic inflammation, and patients with multiple plaque rupture can be expected to show a poor prognosis. Our results suggest that AMI treatment should focus not only on stabilization of the culprit site but also a systemic approach to systemic stabilization of the arteries.     

Impact of coronary artery remodeling on clinical presentation of coronary artery disease: an intravascular ultrasound study

OBJECTIVES: We examined the association between the features of the culprit lesion in coronary artery disease (CAD) and clinical presentation as shown by intravascular ultrasound (IVUS). BACKGROUND: The association between coronary remodeling pattern and clinical presentation of CAD is unclear. METHODS: We analyzed 125 selected patients who underwent preintervention IVUS. Acute myocardial infarction (AMI) and unstable angina pectoris (UAP) were categorized as an acute coronary syndrome (ACS), and stable angina pectoris (SAP) and old myocardial infarction (OMI) as stable CAD. Coronary remodeling patterns and plaque morphology of the culprit lesion obtained by IVUS were analyzed in terms of their association with clinical presentation or angiographic morphology. RESULTS: Angiographically complex lesions were associated with ACS and OMI. In patients with a complex lesion, positive remodeling was observed more frequently than in those with a simple lesion. In AMI and UAP, positive remodeling was observed more frequently than in SAP and OMI (82% vs. 78% vs. 33% vs. 40%, respectively, p < 0.0001). The remodeling ratio was greater in AMI and UAP than in SAP and OMI (1.26 +/- 0.15 vs. 1.11 +/- 0.10 vs. 0.94 +/- 0.11 vs. 0.96 +/- 0.13, respectively, p < 0.0001). Furthermore, within ACS, the remodeling ratio was greater in AMI than in UAP (1.26 +/- 0.15 vs. 1.11 +/- 0.10, respectively, p < 0.05), whereas the frequency of positive remodeling was not different. CONCLUSIONS: Positive remodeling was more frequently observed in ACS than in stable CAD. Moreover, the degree of positive remodeling was greater in AMI than in UAP. These results may reflect the impact of remodeling types and its degree in the culprit lesion of CAD on clinical presentation.     

Increased Vulnerability and Distinct Layered Phenotype at Culprit and Nonculprit Lesions in STEMI Versus NSTEMI

ObjectivesThis study aimed to investigate the pancoronary plaque vulnerability (including culprit and nonculprit lesions) and layered phenotype in patients with ST-segment elevation myocardial infarction (STEMI) vs non-STEMI (NSTEMI).BackgroundPancoronary vulnerability should account for distinct clinical manifestations of acute myocardial infarction (AMI). Layered plaque is indicative of previous coronary destabilization and thrombosis.MethodsA total of 464 patients with AMI who underwent 3-vessel optical coherence tomography imaging were consecutively studied and divided into a STEMI group (318 patients; 318 culprit and 1,187 nonculprit plaques) and a NSTEMI group (146 patients; 146 culprit and 560 nonculprit plaques). Patients were followed up for a median period of 2 years.ResultsCompared with NSTEMI, culprit lesions in STEMI had more plaque rupture, thrombus, thin-cap fibroatheroma (TCFA), calcification, macrophage accumulation, and microvessels. The prevalence of plaque rupture (8.2% vs 4.8%; P = 0.018), microvessels (57.5% vs 45.2%; P < 0.001), and calcification (40.7% vs 30.2%; P = 0.003) at nonculprit lesions was higher in STEMI than NSTEMI. The layer area and thickness at the culprit and nonculprit lesions were significantly larger in STEMI than in NSTEMI. Multivariate analyses showed that culprit layer area (odds ratio: 1.443; 95% CI: 1.138-1.830; P = 0.002) was predictive of STEMI (vs NSTEMI), in addition to culprit TCFA, culprit thrombus, and non–left circumflex artery location of the culprit lesion. Although the type of AMI was not related to clinical outcomes, high-sensitivity C-reactive protein, culprit calcified nodule, and nonculprit TCFA predicted the 2-year major adverse cardiovascular events in patients with AMI.ConclusionsPatients with STEMI had increased plaque vulnerability (ie, more plaque rupture and microvessels) and distinct layered phenotype at the culprit and nonculprit lesions compared with patients with NSTEMI. Culprit lesion features of large layer area, TCFA, thrombus, and non–left circumflex artery location predicted the clinical presentation of STEMI.     

Intravascular ultrasound assessment of the association between spatial orientation of ruptured coronary plaques and remodeling morphology of culprit plaques in ST-elevation acute myocardial infarction

The aim of this study was to assess the association between the spatial location of plaque rupture and remodeling pattern of culprit lesions in acute anterior myocardial infarction (MI). Positive remodeling suggests a potential surrogate marker of plaque vulnerability, whereas plaque rupture causes thrombus formation followed by coronary occlusion and MI. Intravascular ultrasound (IVUS) can determine the precise spatial orientation of coronary plaque formation. We studied 52 consecutive patients with acute anterior MI caused by plaque rupture of the culprit lesion as assessed by preintervention IVUS. The plaques were divided into those with and without positive remodeling. We divided the plaques into three categories according to the spatial orientation of plaque rupture site: myocardial (inner curve), epicardial (outer curve), and lateral quadrants (2 intermediate quadrants). Among 52 plaque ruptures in 52 lesions, 27 ruptures were oriented toward the epicardial side (52%), 18 toward the myocardial side (35%), and 7 in the 2 lateral quadrants (13%). Among 35 plaques with positive remodeling, plaque rupture was observed in 21 (52%) on the epicardial side, 12 (34%) on the myocardial side, and 2 (6%) on the lateral side. However, among 17 plaques without positive remodeling, plaque rupture was observed in 6 (35%), 6 (35%), and 5 (30%), respectively (p?=?0.047). Atherosclerotic plaques with positive remodeling showed more frequent plaque rupture on the epicardial side of the coronary vessel wall in anterior MI than those without positive remodeling.     

Negative remodeling and calcified plaque in octogenarians with acute myocardial infarction: an intravascular ultrasound analysis.

OBJECTIVES: The goal of this study was to use intravascular ultrasound (IVUS) to compare octogenarians versus patients <65 years of age with regard to culprit lesion morphology in acute myocardial infarction (MI). BACKGROUND: Although octogenarians represent the fastest-growing segment of our population and have a higher risk profile, they are underrepresented in therapeutic trials. METHODS: Between 2002 and 2005, 42 octogenarians and 52 patients <65 years of age underwent pre-intervention IVUS within 2 days from onset of an MI. Qualitative and quantitative measurements were performed at the lesion site and at the proximal and distal references. Positive remodeling was defined as a remodeling index (lesion/mean reference arterial area) > or =1. RESULTS: Elderly patients mostly (71%) presented with non-ST-segment elevation myocardial infarction (NSTEMI), whereas patients <65 years of age presented almost equally with ST-segment elevation myocardial infarction (STEMI) and NSTEMI (56% vs. 44%). The frequency of rupture/dissection was greater in the <65-year-old group (32% vs. 9%, p = 0.009), and culprit lesions contained more thrombus in this group (14% vs. 2%, p = 0.04). Conversely, in octogenarians, lesions were predominantly calcified (57% vs. 10%, p < 0.001) and longer (20.9 +/- 7.8 mm vs. 16.6 +/- 6.1 mm, p = 0.004) with less positive remodeling (19% vs. 56%, p < 0.001). On multivariant logistic regression analysis, age was the only independent predictor of calcified plaque (p = 0.02) and remodeling (p = 0.005). CONCLUSIONS: Negative remodeling and calcified plaque with rare plaque ruptured were common in elderly people with acute MI. These findings may contribute to the difference in clinical presentation and may suggest a different pathophysiologic mechanism of MI in octogenarians.     

Intravascular ultrasound findings that are predictive of no reflow after percutaneous coronary intervention for saphenous vein graft disease

The aim of this study was to investigate the relation between intravascular ultrasound (IVUS) findings and the no-reflow phenomenon and long-term outcome after percutaneous coronary intervention (PCI) of saphenous vein graft (SVG) lesions. No reflow was defined as Thrombolysis In Myocardial Infarction grade 0, 1, or 2 flow after PCI. Of 311 patients who underwent IVUS before and after stenting, no reflow was observed in 39 patients (13%). Degenerated SVG (62% vs 36%, p = 0.002), IVUS-detected intraluminal mass (82% vs 43%, p <0.001), culprit lesion multiple plaque ruptures (23% vs 6%, p <0.001), and tissue prolapse (51% vs 35%, p = 0.043) were observed more frequently in patients with no reflow. In multivariate logistic regression analysis, an intraluminal mass (odds ratio [OR] 4.84, 95% confidence interval [CI] 1.98 to 10.49, p = 0.001), culprit lesion multiple plaque ruptures (OR 3.46, 95% CI 1.46 to 8.41, p = 0.014), and degenerated SVGs (OR 3.17, 95% CI 1.17 to 6.56, p = 0.024) were the independent predictors of no reflow after PCI. At 5-year clinical follow-up, rates of death (14, 36%, vs 55, 20%, p = 0.036) and myocardial infarction (13, 33%, vs 52, 19%, p = 0.039) were significantly higher in the no-reflow group. However, rate of target vessel revascularization was not significantly different between the 2 groups (15, 38%, vs 90, 33%, p = 0.3). IVUS-detected intraluminal mass, multiple plaque ruptures, and degenerated SVGs were associated with no reflow in SVG lesions after PCI. In conclusion, no reflow was associated with poor long-term clinical outcomes after PCI for SVG lesions.     

Reperfusion syndrome: relationship of coronary blood flow reserve to left ventricular function and infarct size

OBJECTIVES: We tested the hypothesis that the reperfusion syndrome (RS), defined as an additional elevation of the ST segment upon reperfusion, may be a marker of microcirculatory reperfusion injury during acute myocardial infarction (AMI). BACKGROUND: The pathophysiology of the RS is unknown, and its prognostic implications are controversial. METHODS: Twenty-one patients with an anterior AMI treated < or =12 h after onset by primary coronary angioplasty (PTCA) were studied. Coronary velocity reserve (CVR), an index of microcirculatory function, was measured using a Doppler guidewire. Left ventricular (LV) ejection fraction, infarct size (percent defect) and LV end-systolic volume index (LVESVi) were evaluated by radionuclide ventriculography, 201T1 single-photon emission computed tomography and contrast ventriculography, respectively. RESULTS: Baseline ST elevation and pain-to-TIMI 3 time were similar in patients with and without RS. Patients with RS (10/21) had a lower post-PTCA CVR than patients without RS (median [95% confidence interval]: 1.2 [1-1.3] vs. 1.6 [1.5-1.7], p < 0.005). Even though predischarge CVR was similar in the two groups, infarct size at six weeks (26 [21 to 37] vs. 14 [10-17]% 201T1 defect, p = 0.001) and predischarge LVESVi (45% [40 to 52] vs. 30% [29 to 38] mL/m2, p = 0.001) were larger, and LV ejection fraction at six weeks (40% [37 to 46] vs. 55% [50 to 60], p = 0.004) was lower in patients with RS than in patients without RS. CONCLUSIONS: Patients with RS during primary PTCA for an anterior AMI have a transiently lower CVR than patients without RS, but sustained LV dysfunction and larger infarct size, suggesting that RS is a marker of microcirculatory reperfusion injury.     

Chronic pretreatment of ACEI reduces no-reflow in patients with acute myocardial infarction treated with primary angioplasty

BACKGROUND: In animal models, pretreatment with angiotensin-converting enzyme inhibitor (ACEI) can reduce no-reflow. In the present study, we investigated whether pretreatment with ACEI may prevent no-reflow in patients who underwent primary coronary intervention for AMI. METHOD AND RESULTS: A total of 259 consecutive patients who underwent primary angioplasty for a first AMI were studied. No-reflow was defined as a TIMI flow grade < 3. The no-reflow phenomenon was found in 33 of 259 patients. There were no significant differences in clinical characteristics between the patients with and without ACEI pretreatment. However, the 47 patients receiving chronic ACEI treatment before admission had lower incidence of the no-reflow than those without it (4.2 and 14.6%, p<0.05). Multivariable logistic regression analysis revealed that absence of ACEI pretreatment was a significant predictor of the no-reflow along with absence of preinfarction angina, complete occlusion of the culprit lesion, high-burden thrombus, ejection fraction on admission, number of Q-waves, absence of statin pretreatment, and anterior AMI. CONCLUSION: Pretreatment with ACEI could preserve the microvascular integrity after acute myocardial infarction in humans.     

Endothelin-1 and acute myocardial infarction: a no-reflow mediator after successful percutaneous myocardial revascularization.

AIMS: No-reflow after a primary percutaneous coronary intervention (PCI) is associated with a high incidence of left ventricular (LV) failure and a poor prognosis. Endothelin-1 (ET-1) is a potent endothelium-derived vasoconstrictor peptide and an important modulator of neutrophil function. Elevated systemic ET-1 levels have recently been reported to predict a poor prognosis in patients with acute myocardial infarction (AMI) treated by primary PCI. We aimed to investigate the relationship between systemic ET-1 plasma levels and no-reflow in a group of AMI patients treated by primary PCI. METHODS AND RESULTS: A group of 51 patients (age 59+/-9.9 years, 44 males) with a first AMI, undergoing successful primary or rescue PCI, were included in the study. Angiographic no-reflow was defined as coronary TIMI flow grade < or =2 or TIMI flow 3 with a final myocardial blush grade < or =2. Blood samples were obtained from all patients on admission for ET-1 levels measurement. No reflow was observed in 31 patients (61%). Variables associated with no-reflow at univariate analysis included culprit lesion of the left anterior coronary descending artery (LAD) (67 vs. 29%, P=0.006) and ET-1 plasma levels (3.95+/-0.7 vs. 3.3+/-0.8 pg/mL, P=0.004). At multivariable logistic regression analysis, ET-1 was the only significant predictor of no-reflow (P=0.03) together with LAD as the culprit vessel (P=0.04). CONCLUSION: ET-1 plasma levels predict angiographic no-reflow after successful primary or rescue PCI. These findings suggest that ET-1 antagonists might be beneficial in the management of no-reflow.     

Complete atrioventricular block complicating inferior wall acute myocardial infarction treated with reperfusion therapy. TAMI Study Group

Previous studies report larger myocardial infarcts and increased in-hospital mortality rates in patients with inferior wall acute myocardial infarction (AMI) and complete atrioventricular block (AV), but the clinical implications of these complications in patients treated with reperfusion therapy have not been addressed. The clinical course of 373 patients--50 (13%) of whom developed complete AV block--admitted with inferior wall AMI and given thrombolytic therapy within 6 hours of symptom onset was studied. Acute patency rates of the infarct artery after thrombolytic therapy were similar in patients with or without AV block. Ventricular function measured at baseline and before discharge in patients with complete AV block showed a decrement in median ejection fraction (-3.5 vs -0.4%, p = 0.03) and in median regional wall motion (-0.14 vs +0.24 standard deviations/chord, p = 0.05). The reocclusion rate was higher in patients with complete AV block (29 vs 16%, p = 0.03). Patients with complete AV block had more episodes of ventricular fibrillation or tachycardia (36 vs 14%, p less than 0.001), sustained hypotension (36 vs 10%, p less than 0.001), pulmonary edema (12 vs 4%, p = 0.02) and a higher in-hospital mortality rate (20 vs 4%, p less than 0.001), although the mortality rate after hospital discharge was identical (2%) in the 2 groups. Multivariable logistic regression analysis revealed that complete AV block was a strong independent predictor of in-hospital mortality (p = 0.0006). Thus, despite initial successful reperfusion, patients with inferior wall AMI and complete AV block have higher rates of in-hospital complications and mortality.     

Prediction of no-reflow phenomenon after successful percutaneous coronary intervention in patients with acute myocardial infarction: intravascular ultrasound findings.

Plaque characterization by intravascular ultrasound (IVUS) before percutaneous coronary intervention (PCI) was evaluated in 81 consecutive patients with acute myocardial infarction (AMI) to establish if IVUS can predict the occurrence of the 'no-reflow' phenomenon. Angiographic no-reflow was defined as TIMI flow grade 1 or 2 without any mechanical obstruction in the epicardial artery. Patients were divided into 2 groups according to the post-PCI angiograms: normal flow (group R, n=60) and no-reflow (group NR, n=21). Although the incidence of either soft or noncalcified plaque was not statistically different between the groups, positive vessel remodeling was more frequent in group NR than in group R (57.1% vs 31.6%, p<0.05). Lipid core was also more frequently found in group NR than in group R (61.9% vs 25.0%, p<0.01). Positively remodeled vessels with lipid-rich plaques as characterized by IVUS before PCI predicted the occurrence of angiographic no reflow with a sensitivity of 43% and a specificity of 60%.     

Rupture of the left ventricular free wall during acute myocardial infarction: analysis of 138 necropsy patients and comparison with 50 necropsy patients with acute myocardial infarction without rupture

Clinical and necropsy findings in 138 patients (69 men and 69 women) with rupture of the left ventricular (LV) free wall during acute myocardial infarction (AMI) (rupture group) were compared with 50 patients who died during their first AMI without rupture (nonrupture group). The frequency of systemic hypertension (55 vs 52%), angina pectoris (13 vs 22%) and congestive heart failure (0 vs 0%) before the fatal AMI was similar for both rupture and nonrupture groups. Mean heart weights for men (479 vs 526 g) and women (399 vs 432 g) with and without rupture also were insignificantly different. LV scar before the infarct that ruptured was present in 18 patients (13%); previous necropsy studies of fatal AMI without rupture have indicated that 50% have LV scars. The rupture group had a significantly more frequent (p less than 0.01) lateral wall location of the infarct (12 vs 2%). The number of 3 major (right, left anterior descending and left circumflex) epicardial coronary arteries narrowed at some point greater than 75% in cross-sectional area by atherosclerotic plaque was significantly lower (p less than 0.01) in the rupture group (39 vs 58%). The percent of these 3 arteries totally occluded or nearly so (greater than 95% in cross-sectional area) by plaque also was significantly less (p less than 0.001) in the rupture group (24 of 198 arteries [12%] vs 38 of 144 arteries [26%]). Analysis of each 5-mm long segment of these arteries in each group disclosed that the rupture group had significantly less narrowing than the nonrupture group. Of the 3,287 five-mm segments of artery examined in the rupture group (66 patients), 512 (15%) were narrowed greater than 75% in cross-sectional area by plaque; in contrast, of the 1,848 five-mm segments in the nonrupture group (38 patients), 508 (28%) were narrowed to this degree by plaque (p less than 0.0001). Thus, rupture of the LV free wall primarily is a complication of the first AMI and is associated with considerably less amounts of coronary narrowing than fatal AMI without rupture.